There have been remarkable recent advances in knowledge about
duodenal ulcer, a disease which may be spontaneously disappearing. Multiple physiologic defects have been found including increased numbers of parietal cells and their increased sensitivity to
gastrin, excessive
gastrin release after food intake, decreased inhibition of
gastrin release by low
antral pH, more rapid gastric emptying, and, possibly, impaired duodenal mucosal resistance to
acid.
Antacid and
diet therapies have been subjected to scientific scrutiny and their respective roles in the
therapy of the
duodenal ulcer are now better defined. New drugs have been developed which strongly inhibit gastric acid secretion in man--the recently marketed
histamine H2-receptor antagonist,
cimetidine, as well as chemically modified
prostaglandins. Clinical trials have shown
cimetidine to be effective in healing
duodenal ulcers and free of significant side effects with short-term usage. Its role in the prevention of
ulcer recurrence is presently being evaluated. A new operation for
duodenal ulcer has been introduced which shows great promise following pilot studies and some randomized trials. Only the parietal cell containing portion of the stomach is denervated. Basal and stimulated gastric acid secretion are markedly inhibited while gastric motility is unimpaired. This operation thus eliminates the need for a drainage procedure or distal
antral resection and decreases the incidence and severity of undesirable side effects associated with earlier operations for
duodenal ulcer.